β2-glycoprotein I (β2-GPI) mRNA is expressed by several cell types involved in anti-phospholipid syndrome-related tissue damage

Caronti, Brunella; Calderaro, Caterina; Alessandri, Cristiano; Conti, Fabrizio; Tinghino, Raffaella; Palladini, Giovanni; Valesini, Guido

doi:10.1046/j.1365-2249.1999.00770.x

Cited by 68 publications

(54 citation statements)

References 43 publications

(60 reference statements)

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“…Although it is generally accepted that the protein is present on different endothelial cell membranes (50,51), the results on apoH mRNA expressed by endotheliocytes are conflicting (39,40). Moreover, we did not observe apoH transcripts in endothelial cells.…”

Section: Discussioncontrasting

confidence: 74%

“…More recently apoH mRNA was found by RT-PCR on RNA extracted from other tissues (intestine, placenta, foetal astrocytes, lymphocytes) or cultured cells (transformed cell lines) such as choriocarcinoma, hepatoma (36), colon adenocarcinoma (35), neuroblastoma, umbilical vein endothelial cells (HUVEC, but not for Alvarado-de la Barrera, 39), astrocytoma, glioblastoma cells (40) and in monocytes (41).…”

Section: Introductionmentioning

confidence: 99%

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RT-PCR and in situ hybridization analysis of apolipoprotein H expression in rat normal tissues

Ragusa

Costa²,

Cefalù³

et al. 2006

Int J Mol Med

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Abstract. In this study, by using different techniques (i.e. Northern blot hybridization, RT-PCR and Southern blot hybridization) on various normal rat tissues, we were able to identify liver, kidney, heart, small intestine, brain, spleen, stomach and prostate as tissues in which the ApoH gene is transcribed. Moreover, for some of these tissues, by in situ hybridization, we found a specific localization of apoH transcripts. For instance epithelial cells of the bile ducts in liver and of the proximal tubules in kidney are the major sites of apoH synthesis. Our data suggest that some of the different physiological roles proposed for apoH could correlate with its direct expression, while others could correlate with its absorption from bloodstream or adjacent cells.

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Section: Discussioncontrasting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

RT-PCR and in situ hybridization analysis of apolipoprotein H expression in rat normal tissues

Ragusa

Costa²,

Cefalù³

et al. 2006

Int J Mol Med

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“…The best described antigen in APS is β-2 glycoprotein I (β 2 GPI). β 2 GPI, a cationic lipid-binding protein with unclear function, is made especially by the liver and circulates at high levels in plasma (50-200 μg/ml) (6,7). It has been suggested that anti-β 2 GPI antibodies potentiate thrombosis by engaging β 2 GPI on cell surfaces, thereby promoting cell activation (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Activated signature of antiphospholipid syndrome neutrophils reveals potential therapeutic target

et al. 2017

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“…[8][9][10] Another property of ␤ 2 -GPI is its ability to bind at the monocyte surface, thus promoting tissue factor and thereby increasing the risk of thrombotic events. 11 ␤ 2 -GPI can also be expressed on the endothelial cell membrane 12 and on macrophages. 13 Among the several candidate ␤ 2 -GPI cell receptors, annexin II, megaline, and apolipoprotein E receptor 2Ј (apoER2Ј) are involved in activating endothelial cells and platelets.…”

Section: Introductionmentioning

confidence: 99%

Oxidized β2-glycoprotein I induces human dendritic cell maturation and promotes a T helper type 1 response

Buttari

Profumo

Mattei

et al. 2005

Blood

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The human plasma protein ␤ 2 -glycoprotein I (␤ 2 -GPI) is the most common target for antiphospholipid antibodies associated with thrombotic events in chronic disorders related to endothelial cell dysfunction. Crucial information is needed to clarify why this self-abundant protein is targeted by autoimmune responses. In this study, we investigated whether oxidative modification of ␤ 2 -GPI, either spontaneous in culture wells or induced by treatment with H 2 O 2 , renders this selfprotein able to activate immature monocyte-derived dendritic cells (DCs) from healthy human donors. Oxidized ␤ 2 -GPI caused DCs to mature so that CD83 appeared and CD80, CD86, human leukocyte antigen-D region related (HLA-DR), and CD40 increased. The interaction between oxidized ␤ 2 -GPI and DCs specifically stimulated these cells to secrete interleukin 12 (IL-12), IL-1␤, IL-6, IL-8, tumor necrosis factor ␣ (TNF-␣), and IL-10. Oxidized ␤ 2 -GPI-stimulated DCs had increased allostimulatory ability and primed naive T lymphocytes, thus inducing T helper 1 (Th1) polarization. The interaction between oxidized ␤ 2 -GPI and DCs involved interleukin-1 receptor associated kinase (IRAK) phosphorylation and nuclear factor B (NFB) activation. Pretreatment of ␤ 2 -GPI with the antioxidant ␣-tocopherol prevented DC maturation. These findings show that human oxidized ␤ 2 -GPI, probably by interacting with a member of the Toll-like receptor (TLR) family, causes DCs to mature. Because this key ␤ 2 -GPI function requires oxidative modification, in several chronic disorders related to endothelial cell dysfunction oxidative stress might trigger the "autoimmune spiral. Introduction␤ 2 -glycoprotein I (␤ 2 -GPI), a human plasma protein that binds to negatively charged phospholipids, is the most common target for antiphospholipid antibodies (aPLs). These autoantibodies are associated with thrombotic events in systemic lupus erythematosus 1 and primary antiphospholipid antibody syndrome 2,3 and are proatherogenic. 4 ␤ 2 -GPI also activates lipoprotein lipase, 5 lowers the triglyceride level, 6 and binds to oxidized low-density lipoprotein (LDL) 7 and to nonself particles or apoptotic bodies to allow their clearance. [8][9][10] Another property of ␤ 2 -GPI is its ability to bind at the monocyte surface, thus promoting tissue factor and thereby increasing the risk of thrombotic events. 11 ␤ 2 -GPI can also be expressed on the endothelial cell membrane 12 and on macrophages. 13 Among the several candidate ␤ 2 -GPI cell receptors, annexin II, megaline, and apolipoprotein E receptor 2Ј (apoER2Ј) are involved in activating endothelial cells and platelets. [14][15][16] Recent findings demonstrate that anti-␤ 2 -GPI antibodies react with their antigen probably in association with a member of the Toll-like receptor (TLR)/interleukin 1 (IL-1) receptor family on the endothelial cell surface and directly induce activation. 17,18 Once bound to endothelial cells, ␤ 2 -GPI offers suitable epitopes targeting circulating anti-␤ 2 -GPI antibodies that affect cell functions a...

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β2-glycoprotein I (β2-GPI) mRNA is expressed by several cell types involved in anti-phospholipid syndrome-related tissue damage

Cited by 68 publications

References 43 publications

RT-PCR and in situ hybridization analysis of apolipoprotein H expression in rat normal tissues

RT-PCR and in situ hybridization analysis of apolipoprotein H expression in rat normal tissues

Activated signature of antiphospholipid syndrome neutrophils reveals potential therapeutic target

Oxidized β2-glycoprotein I induces human dendritic cell maturation and promotes a T helper type 1 response

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